Reflux of upper intestinal content in general and of bile acids in particular has been implicated in the development of acute and chronic gastric mucosal disease, specifically, acute post-traumatic hemorrhagic gastritis, type I benign gastric ulcer, and post-operative alkaline reflux gastritis. The present request proposes to examine in the experimental laboratory the pathophysiology of these disease entities by investigating (1) the influence of tissue ATP content on bile acid induced acute gastric mucosal ulcerogenesis, (2) the influence of pH on the same parameter, (3) the susceptibility of atrophic gastric mucosa to acute gastric mucosal ulcerogenesis, (4) the degree and duration of ischemia required to induce acute mucosal damage in a proven laboratory mode, (5) the role of endogenous acid in the production of acute gastric mucosal lesions induced by bile acids and ischemia, (6) the susceptibility of denervated antral mucosa to acute mucosal ulcerogenesis, (7) the influence of pH on bile acid induced alterations in gastric mucosal nutrient blood flow, (8) the effect of chronic bile acid application on mucosal histology and function in both antrum and fundus, and, (9) the effect of topical bile acid application on tissue water content and distribution. In a related clinical study of post-operative alkaline reflux gastritis, the present request proposes to define that syndrome more precisely by quantitating differences between symptomatic and asymptomatic post-gastrectomy patients in the following areas: (1) the magnitude of bile acid regurgitation into the residual gastric pouch, (2) the specific fractions of bile acids refluxed, (3) the capacity of the residual gastric pouch to produce acid, (4) serum levels of specific circulating gastric mucosal trophic factors, (5) the quantity of ingested anti-inflammatory drugs, and, (6) the magnitude of gastroscopic gastritis present.